The purpose of this research project is to investigate the mechanism of the putative satiety signal, cholecystokinin (CCK). This hormone is released into the blood by food acting on the surface of the intestine. There is good evidence that CCK plays an important role in terminating a meal and eliciting satiety behavior in both intact and sham feeding rats. The mechanism and site of action, however, are not known. We are proposing two experiments which will indicate whether CCK acts directly or indirectly on the brain to elicit satiety. In the first experiment, CCK will be infused into the brain through the carotid circulation while the animals are feeding. Analysis of the dose related satiety effect by this route of administration will reveal a central CCK "satiety receptor" if one exists. The second alternative is that CCK affects the brain indirectly by arousing afferent activity in peripheral nerves. To examine this possibility, animals will be tested for the CCK satiety effect after vagotomy, sympathectomy, and total deafferentation of the viscera below the diaphragm. This experiment will indicate whether or not the peripheral autonomic afferent nerves are necessary for the CCK satiety effect.